Rubella natural history

Rubella Microchapters

Home

Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Differentiating Rubella from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Treatment

Medical Therapy

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Case Studies

Case #1

Rubella natural history On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Rubella natural history

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Rubella natural history

CDC on Rubella natural history

Rubella natural history in the news

Blogs on Rubella natural history

Directions to Hospitals Treating Rubella

Risk calculators and risk factors for Rubella natural history

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Michael Maddaleni, B.S.

## Contents

* 1 Overview
* 2 Natural history
* 3 Complications
* 4 Prognosis
* 5 References

## Overview

[edit | edit source]

## Natural history

[edit | edit source]

Rubella was first described in the mid-eighteenth century. Friedrich Hoffmann made the first clinical description of rubella in 1740,[1] which was confirmed by de Bergen in 1752 and Orlow in 1758.[2]

In 1814, George de Maton first suggested that it be considered a disease distinct from both measles and scarlet fever. All these physicians were German, and the disease was known as Rötheln (from the German name Röteln), hence the common name of "German measles". [3] Henry Veale, an English Royal Artillery surgeon, described an outbreak in India. He coined the name "rubella" (from the Latin, meaning "little red") in 1866.[1][4][5][6]

It was formally recognised as an individual entity in 1881, at the International Congress of Medicine in London.[7] In 1914, Alfred Fabian Hess theorised that rubella was caused by a virus, based on work with monkeys.[8] In 1938, Hiro and Tosaka confirmed this by passing the disease to children using filtered nasal washings from acute cases.[5]

In 1940, there was a widespread epidemic of rubella in Australia. Subsequently, ophthalmologist Norman McAllister Gregg found 78 cases of congenital cataracts in infants and 68 of them were born to mothers who had caught rubella in early pregnancy.[4][5] Gregg published an account, Congenital Cataract Following German Measles in the Mother, in 1941. He described a variety of problems now know as congenital rubella syndrome (CRS) and noticed that the earlier the mother was infected, the worse the damage was. The virus was isolated in tissue culture in 1962 by two separate groups led by physicians Parkman and Weller.[6][4]

There was a pandemic of rubella between 1962 and 1965, starting in Europe and spreading to the United States.[6] In the years 1964-65, the United States had an estimated 12.5 million rubella cases. This led to 11,000 miscarriages or therapeutic abortions and 20,000 cases of congenital rubella syndrome. Of these, 2,100 died as neonates, 12,000 were deaf, 3,580 were blind and 1,800 were mentally retarded. In New York alone, CRS affected 1% of all births [9]

In 1969 a live attenuated virus vaccine was licensed.[5] In the early 1970s, a triple vaccine containing attenuated measles, mumps and rubella (MMR) viruses was introduced.[6]

## Complications

[edit | edit source]

Rubella can cause a wide variety of problems that are seen very commonly with rubella or not very often at all. Two of the more common complications that occur with the rubella virus are arthralgia and arthritis. For currently unknown reasons, the symptoms that were just mentioned are found to be more prevalent in women with the rubella virus than with men with the rubella virus[10]. There are also some more serious complications associate with the rubella virus. One of these complications is thrombocytopenic purpura, which is a disorder with the blood. It causes extensive microscopic clots to form in the small blood vessels of the body. Before effective treatment was developed, the fatality rate was approximately 90%.

Another complication associated with the rubella virus is postinfectious encephalopathy or encephalomyelitis. Encephalomyelitis is basically just a general term for inflammation of the brain and spinal cord. It should be noted, though, that encephalomyelitis and thrombocytopenic purpura are rarely associated with postnatally developed rubella[10].

Probably the most major concern, and public health concern, associated with rubella is its teratogenicity. The length of gestation when a mother contracts rubella plays a major factor in determining which congenital defects may be possible. If the woman contracts rubella earlier in her pregnancy, then there is a higher chance of her child developing serious defects[10]. Nearly 100% of fetuses become infected when a mother contracts the disease within the first 8 weeks of pregnancy[10]. After approximately 17 weeks (the first trimester), contracting rubella will most likely not have consequences on the child.

Some of the complications that have been reported with the child include[10]. :

* Deafness
* Cardiac disease
* Mental retardation
* Ocular conditions including
* Cataracts
* Glaucoma
* Insulin dependent diabetes mellitus

It should be noted that there have been no cases reported of rubella infection causing congenital rubella syndrome after 12 weeks gestation.

## Prognosis

[edit | edit source]

Rubella infection of children and adults is usually mild, self-limiting and often asymptomatic. The prognosis in children born with CRS is poor.[11]

## References

[edit | edit source]

1. ↑ 1.0 1.1 Ackerknecht, Erwin Heinz (1982). A short history of medicine. Baltimore: Johns Hopkins University Press. p. 129\. ISBN 0-8018-2726-4.
2. ↑ Wesselhoeft C (1949). "Rubella and congenital deformities". N. Engl. J. Med. 240 (7): 258–61. PMID 18109609.
3. ↑ Best, J.M., Cooray, S., Banatvala J.E. Rubella in Topley and Wilson's Microbiology and Microbial Infections, Vol. 2, Virology, Chapter 45, p.960-92, ISBN 0 340 88562 9, 2005
4. ↑ 4.0 4.1 4.2 Lee JY, Bowden DS (2000). "Rubella virus replication and links to teratogenicity". Clin. Microbiol. Rev. 13 (4): 571–87. PMID 11023958.
5. ↑ 5.0 5.1 5.2 5.3 Atkinson W, Hamborsky J, McIntyre L, Wolfe S, eds. (2007). "Chapter 12. Rubella". Epidemiology and Prevention of Vaccine-Preventable Diseases. 10th ed. Centers for Disease Control and Prevention. Retrieved 2007-07-03. Unknown parameter `|chapterURL=` ignored (`|chapterurl=` suggested) (help)CS1 maint: Multiple names: authors list (link) CS1 maint: Extra text: authors list (link)
6. ↑ 6.0 6.1 6.2 6.3 "Chapter 11 - Rubella". Immunisation Handbook 2006. Ministry of Health, Wellington, NZ. 2006. ISBN 0-478-29926-5. Retrieved 2007-07-03. Unknown parameter `|month=` ignored (help); Unknown parameter `|chapterURL=` ignored (`|chapterurl=` suggested) (help)
7. ↑ Smith, J. L. Contributions to the study of Rötheln. Trans. Int. Med. Congr. Phil. 4,14. 1881
8. ↑ Hess, Alfred Fabian (1914). "German measles (rubella): an experimental study". The Archives of Internal Medicine. Chicago. 13: 913–916. as cited by Enersen, Ole Daniel. "Alfred Fabian Hess". WhoNamedIt. Retrieved 2007-07-03.
9. ↑ J.B. Hanshaw, J.A. Dudgeon, and W.C. Marshall. Viral diseases of the fetus and newborn. W.B. Saunders Co., Philadelphia, 1985
10. ↑ 10.0 10.1 10.2 10.3 10.4 Lee JY, Bowden DS (2000). "Rubella virus replication and links to teratogenicity". Clinical Microbiology Reviews. 13 (4): 571–87. PMC 88950. PMID 11023958. Retrieved 2012-02-09. Unknown parameter `|month=` ignored (help)
11. ↑ Freij BJ, South MA, Sever JL (1988). "Maternal rubella and the congenital rubella syndrome". Clin Perinatol. 15 (2): 247–57. PMID 3288422.CS1 maint: Multiple names: authors list (link)

complications and prognosis